Abstract
Background:
Centromere protein N (CENPN), a member of the centromere protein family, contributes to ribonucleic assembly, mitosis progression, and chromosome separation. CENPN manifests a close link with the occurrence and progression of several malignant cancers, but there is no pan-cancer study on CENPN, and we aim to ascertain the connection between CENPN and human cancer prognosis and immunotherapy.
Methods:
The CENPN function in multiple malignant tumors was comprehensively investigated with data from The Cancer Genome Atlas (TCGA) and integrated Gene Expression Omnibus (GEO) database. We examined the transcriptional level, prognostic effect, diagnostic value, genetic and epigenetic alteration, methylation level, and immunological importance of CENPN. Furthermore, this work provided further confirmation of the phenotypic regulating function of CENPN in breast cancer (BC) cells.
Results:
CENPN exhibited significant upregulation in diverse cancer tissues and had different expression patterns across immunological and molecular subgroups in several cancer types. Elevated expression of CENPN may correlate with a worse prognosis. CENPN effectively differentiates most cancers from healthy tissues. Hypomethylate was shown to be CENPN promoter in most cancers. CENPN was shown to be connected with levels of different immune cell infiltration. Kyoto Encyclopedia of Genes and Genomes (KEGG) and the Gene Set Enrichment Analysis (GSEA) analysis suggested that CENPN may mediate neutrophil extranuclear trap formation, cell cycle, and P53 signaling pathways in cancer. In vitro studies showed that the overexpression of CENPN promotes the proliferation, invasion, and migration of BC cells, while concurrently inhibiting their apoptosis.
Conclusions:
CENPN may operate as a novel predictive indicator and molecular target for targeted therapy in pan-cancer. Significantly, CENPN contributed to controlling the BC growth and advancement.
Keywords:
Pan-cancer; cell cycle; centromere protein N (CENPN); methylation; tumor immunity.